ArticleCell transplantation2017
Suppression of Trim32 Enhances Motor Function Repair after Traumatic Brain Injury Associated with Antiapoptosis.
Article in Cell transplantation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- TRIM32 Inhibits NEK7 Ubiquitylation-Dependent Microglia Pyroptosis After Spinal Cord Injury.Molecular biotechnology · 2025Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- Tripartite Motif Protein Family in Central Nervous System Diseases.Cellular and molecular neurobiology · 2023Review
- It's a TRIM-endous view from the top: the varied roles of TRIpartite Motif proteins in brain development and disease.Frontiers in molecular neuroscience · 2023Review
- Whole Exome Sequencing Study Identifies Novel Rare Risk Variants for Habitual Coffee Consumption Involved in Olfactory Receptor and Hyperphagia.Nutrients · 2022Article
- TRIM32 Inhibition Attenuates Apoptosis, Oxidative Stress, and Inflammatory Injury in Podocytes Induced by High Glucose by Modulating the Akt/GSK-3β/Nrf2 Pathway.Inflammation · 2022Article
- Reducing Neuron Apoptosis in the Pontine Micturition Center by Nerve Root Transfer for Restoration of Micturition Function after Spinal Cord Injury.BioMed research international · 2020Article
- Knockdown of TRIM32 Protects Hippocampal Neurons from Oxygen-Glucose Deprivation-Induced Injury.Neurochemical research · 2019Article
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6 authors.
Funding
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Abstract
To investigate the role of Trim32 in traumatic brain injury (TBI), adult male Sprague Dawley (SD) rats and mice were randomly divided into sham (n = 6) and TBI groups ( n = 24), respectively. Then, mice were assigned into Trim32 knockout mice (Trim32-KO [+/-]) and wild-type (WT) littermates. The TBI model used was the Feeney free-falling model, and neurological function was evaluated after TBI using a neurological severity score (NSS). Reverse transcription polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry were used to investigate the expression of Trim32 in the damaged cortex. Cell apoptosis in the cortex was detected by terminal-deoxynucleoitidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Moreover, Trim32-KO (+/-) mice were used to determine the effect of Trim in neurological repair after TBI. Results showed the NSS scores in TBI rats were significantly increased from day 1 to day 11 postoperation, compared with the sham group. Trim32 messenger RNA (mRNA) expression in the cortex was significantly increased at 7 d after TBI, while the level of Tnr and cytochrome c oxidase polypeptide 5A mRNA didn't exhibit significant changes. In addition, Western blot was used to detect the level of Trim32 protein in the cortex. Trim32 expression was significantly increased at 7 d after TBI, and immunoreactive Trim32-positive cells were mainly neurons. Moreover, Trim32-KO (+/-) mice with TBI had lower NSS scores than those in the WT group from day 1 to day 11 postoperation. Meanwhile, Trim32-KO (+/-) mice had a decreased number of TUNEL-positive cells compared with the control group at 3 d postoperation. Protein 73 (p73) decreased at 7 d postoperation in Trim32-KO (+/-) mice with TBI, when compared with WT mice with TBI. Our study is the first to confirm that suppression of Trim32 promotes the recovery of neurological function after TBI and to demonstrate that the underlying mechanism is associated with antiapoptosis, which may be associated with p73.
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